Fig. 6.12  Biomechanical vectors in midface trauma. The vectors are diverted by the orbital walls and converge to the apex of the orbit (mod. a. Hardt and Steinhaeuser 1979). 1 Complex central midface fracture/central naso-orbito-ethmoidal fracture, 2 cranio-orbital fracture/frontobasal fracture, 3 complex lateral midface fracture

6.1.2.2  Injuries at the Cranio-Orbital Junction

Midface fractures on a high level in combination with orbital wall fractures can cause serious mechanical and neurogenic ophthalmologic complications (Herrmann

a

1976; Holt and Holt 1983; Brent and May 1990; Al-Qurainy et al. 1991a, c; Hardt and Sgier 1991; Fonseca and Walker 1991; Soparkar 2005).

Fractures in the roof of the orbit, especially in the region of the cranio-orbital junction are caused by dislocated lateral midface fractures running through the greater wing of the sphenoid, by cranial fractures with depression of fragments and also by complex central midface fractures through the lesser wing of the sphenoid (Hardt and Steinhäuser 1979; Leider and Mathog 1995) (Fig. 6.12).

Fractures of the greater and lesser wing of the sphenoid can traumatize the cranial nerves III to VI, as they pass through the skull base into the orbit. The optic nerve may also be damaged to a varying degree (Manfredi et al. 1981; Ghobrial et al. 1986; Hardt and Sgier 1991; Leider and Mathog 1995).

Neurological damage is caused by direct compression, by bony fragments or by an indirect compression of the nerves caused by hemorrhage (Rowe and Williams 1985).

Reduced motility of the globe (nerves III, IV, VI) results from fractures in the area of the superior orbital fissure or the roof of the orbit and can lead to rare, but typical ophthalmologic syndromes (Kretschmer 1978; Fonseca and Walker 1991; Dutton and Al-Qurainy 1991) (Fig. 6.13).

Based on the neurological deficits, different orbital syndromes can be distinguished (Hardt and Steinhaeuser 1979; Hardt and Sgier 1991; Dutton and-Al Qurainy 1991):

b

13

14

Fig. 6.13  (a) Coronal section through the superior orbital fissure (with entering cranial nerves and vessels) and the lesser wing of sphenoid (with optic canal) (mod. a. Ghorbial et al. 1986, Hardt and Sgier 1991). (b) Compression of nerves and vascular structures of the superior orbital fissure by displaced bone fragments of the lesser wing of the sphenoid. 1 Optic

nerve, 2 ophthalmic artery, 3 annulus tendinosus (Zinns tendon), 4 lacrimal nerve, 5 frontal nerve 6 superior ophthalmic vein, 7 trochlear nerve, 8 occulomotor nerve, 9 nasociliary nerve, 10 abducent nerve, 11 oculomotor nerve, 12 inferior ophthalmic vein, 13 lesser wing of sphenoid, 14 superior orbital fissure

Distinction between the syndromes according to fracture types show that in most cases the OFS and the HCS are caused by lateral and also centrolateral midface fractures. The OAS and the NOS result mostly from isolated or central midface fractures with cranio­ -orbito-ethmoidal fractures and penetration injuries (Hardt and Sgier 1991) (Fig. 6.14).

Superior Orbital Fissure Syndrome (SOFS)

Dislocated bony fragments or comminuted fractures in the region of the superior orbital fissure or of the lesser wing of the sphenoid cause direct nerve lesions. If all cerebral nerves entering at this point are involved a complete superior orbital fissure syndrome results.

The Complete SOFS

The complete SOFS results from a paresis of the cerebral nerves III, IV, and VI. Clinically there is an ophthalmoplegia with ptosis and an exophthalmus due to disruption of the venous drainage. In addition, a mydriasis and an accommodation paralysis (cycloplegia) occur due to loss of the parasympatic innervation.

If the abducent nerve is still intact, abduction of the eyeball may still be possible (Hedstrom et al. 1974).

Anesthesia in the areas of sensory innervation is inevitable if the sensory branches of the ophthalmic nerve are involved. A severe retroorbital pain sometimes occurs in combination with a supraorbital neurogenic pain as a result of the complex damage that has occurred (Hardt and Sgier 1991).

As a consequence of fragment dislocation, decompression of the orbital fissure via the fronto-temporal access is necessary (Mathog et al. 1995) (Fig. 6.15).

Symptoms

•Complete ophthalmoplegia (nerves III, IV, VI)

•Ptosis

•Mydriasis - accommodation paralysis (cycloplegia)

•Loss of sensibility (ophthalmic, nasociliary nerve)

•Retroorbital pain

•Possible abduction of the eyeball

Incomplete SOFS

Due to the fact that three oculomotor nerves enter through the superior orbital fissure, injuries to the individual branches may lead to a selective paresis, so developing the image of a partial SOFS. Frequent injuries occur in the caudal region of the superior orbital fissure. The clinical loss is usually limited to restriction of the vertical motility of the eyeball due to partial damage of the nerves III and IV, a ptosis, an abnormal pupil reaction and anesthesia in the innervation area of the nasociliar nerve (Hardt and Sgier 1991). Isolated damage to the parasympatic element of the third cerebral nerve leads to a temporary mydriasis, this occurs relatively often in lateral midface fractures (Fig. 6.16).

Symptoms

•Partial ophthalmoplegia (nerves III and/or IV)

•Ptosis

•Mydriasis

•Accommodation paralysis (cycloplegia)

Hemorrhagic Compression Syndrome (HCS)

Massive retrobulbar hemorrhage in the posterior region of the muscle cone, triggered by vessel disruption, leads to progressive exophthalmus with concurrent pupil dilatation, reduced vision and increased intraocular pressure (Ord 1981; Ord and El Altar 1982).

This is a consequence of complex lateral and centrolateral midface fractures and rarely of dislocated fractures in the region of the orbital apex (Hardt and Sgier 1991). Hemorrhage, which causes an increase in intraorbital pressure results in indirect nerve injuries, especially to the optic nerve. These injuries can only be prevented by speedy decompression of the retroorbital hematoma (Rowe 1977; Alper and Aitken 1988; Hardt and Sgier 1991) (Figs. 6.17–6.19).

The following are typical signs of an intraorbital hemorrhage with or without orbital fracture (Doden and Schnaudigel 1978):

•Livid (cyanotic) swollen eyelids with narrow spontaneous palpebral lid opening, which may be opened actively, though passive opening is only slight

•Protrusion of the globe (up to 10 mm) with increasing active and passive immobility

•Increased intra-ocular pressure up to 80 mmHg (normal pressure 20 mmHg)

•Ischemia of the optic disk and retina with clearly reduced vision or amaurosis

•General symptoms similar to the Aschner-symptom- complex (bradycardia, nausea, sweating caused by vagal impulses)

Symptoms

•Complete/incomplete ophthalmoplegia

•Progressive, massive exophthalmus

•Mydriasis

•Vomiting (oculo-gastral reflex)

It is essential to decompress all retrobulbar hematomas with reduced vision, ischemia of the optic papilla and retina, with high intraocular pressure and progressive or manifest exophthalmus in order to prevent permanent damage to the optic nerve (Krausen et al. 1981; Gellrich 1999). The decompression is performed via the transfacial-latero-orbital or transfacial-transeth- moidal approach (Hardt and Sgier 1991; Mathog 1992; Rochels and Rudert 1995) (Fig. 6.20).

Compression in the region of the orbital apex can also be caused by:

•Inwards shifting of the orbital wall (blow-in fracture)

•Subperiostal hematoma (persistent), leading to a reduction of the intraorbital volume and exophthalmus

•Orbital compartment syndrome (any sudden increase in orbital pressure, mostly caused by acute arterial bleeding (ethmoidal artery) or an emphysema)

Orbital Apex Syndrome (OAS)

If retroorbital fractures not only affect the superior orbital fissure, but lead to an immediate lesion of the optic nerve an OAS develops (Brent and May 1990; Radtke and Zahn 1991).

In this case, a high-grade loss of visual acuity or an amaurotic complete iridoplegia occurs. In addition, there is paresis of the three cranial nerves III, IV, and VI (Lisch 1976; Hardt and Sgier 1991; Stewart and Soparkar 2005; Soparkar 2005) (Fig. 6.21).